Adipo-B Index as a Novel Predictor of Beta-Cell Secretory Function Without Measuring Insulin: Cross-Therapeutic Validation Against C-Peptide Index in Treatment-Naïve Type 2 Diabetes

The adipo-B index (adipo-IR divided by HOMA-B) was introduced as an integrator of adipose tissue insulin resistance and pancreatic beta-cell function. Algebraic simplification reveals that insulin cancels from the formula, yielding FFA × (FBG–63)/360 — a composite of circulating free fatty acids and ambient glycemia. We investigated whether this index predicts beta-cell secretory capacity measured by HOMA-B and C-peptide index (CPR-index) across four therapeutic strategies.

RESEARCH DESIGN AND METHODS

A total of 253 treatment-naïve subjects with T2DM received monotherapy with modified Japanese diet for diabetes (MJDD, n=61), canagliflozin (n=67), pioglitazone (n=62), or sitagliptin (n=63). Correlations between baseline adipo-B and baseline beta-cell indices, and between their longitudinal changes, were examined. This is a prospective, non-randomized observational study.

RESULTS

At baseline, adipo-B showed significant negative correlations with HOMA-B with all the subjects. At 3 months, adipo-B significantly decreased and HOMA-B significantly increased with all the therapeutic groups. CPR-index significantly improved with canagliflozin and sitagliptin. Pioglitazone showed a trend toward improvement while MJDD demonstrated no changes. Changes in adipo-B (Δadipo-B) significantly and negatively correlated with changes in both HOMA-B and CPR-index in MJDD, canagliflozin, and sitagliptin. With pioglitazone, no such correlations were observed — consistent with the previously reported bidirectional regulation of insulin secretion by pioglitazone depending on baseline insulin secretory status.

CONCLUSIONS

The adipo-B index predicted beta-cell secretory capacity — assessed independently by conventional beta-cell indices — without requiring insulin or C-peptide measurement. These findings suggest adipo-B may serve as a cost-effective surrogate for assessment of beta-cell function in routine clinical settings.

ARTICLE HIGHLIGHTS

• Why did we undertake this study?

  Insulin cancels algebraically from the adipo-B formula, questioning its validity. We tested if adipo-B predicts beta-cell function using the insulin-independent C-peptide index.

• What is the specific question we wanted to answer?

  Does adipo-B predict beta-cell secretory capacity (via HOMA-B and C-peptide index) without requiring insulin or C-peptide measurements?

• What did we find?

  Cross-sectionally, baseline adipo-B negatively correlated with HOMA-B and CPR-index. Longitudinally, Δadipo-B negatively correlated with ΔHOMA-B and ΔCPR-index for MJDD, canagliflozin, and sitagliptin—but not pioglitazone, reflecting its bidirectional beta-cell regulation.

• What are the implications?

  Adipo-B predicts beta-cell capacity without insulin or C-peptide testing, offering a cost-effective surrogate for routine and resource-limited clinical settings.